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Biomedical subjects

J M Gutteridge

Publications and source records attributed to J M Gutteridge.

At least 181 records · Page 10Linked to original sources
PubMed1982

Free-radical damage to lipids, amino acids, carbohydrates and nucleic acids determined by thiobarbituric acid reactivity.

1. The thiobarbituric acid (TBA) reaction, widely applied to the detection of autoxidation in polyunsaturated fatty acids, can be used to measure free-radical damage to amino acids, carbohydrates and nucleic acids. 2. In all of these systems malondialdehyde (MDA) is predominately formed from intermediate precursor molecules which break down during the acid-heating stage of the TBA test. 3. The acid reagent used to bring about these decompositions appears to be critical.

Amino Acids↗
PubMed1982

Iron-dependent free radical damage to DNA and deoxyribose. Separation of TBA-reactive intermediates.

1. Iron-dependent free radical damage to DNA and deoxyribose results in the formation of thiobarbituric acid (TBA) reactive intermediates. 2. These intermediates have been compared chromatographically and spectrophotometrically after incubation with the enzymes xanthine oxidase and peroxidase. 3. Loss of TBA-reactivity occurred in the bleomycin-iron(II) derived products incubated with xanthine oxidase and in a standard solution of sodium malondialdehyde incubated with peroxidase.

Animals↗
PubMed1982

Detection by fluorescence of peroxides and carbonyls in samples of arachidonic acid.

1 Products of lipid peroxidation were compared in two different grades of commercially-obtained arachidonic acid. 2 The less pure 90% sample was yellow in colour, had low reactivity with 2-thiobarbituric acid and diene conjugation but high u.v. fluorescence, whereas the 99% pure sample, which was clear in colour, showed a reverse pattern of oxidation products. 3 The significance of these findings is discussed.

Arachidonic Acids↗
PubMed1981

The importance of iron in rheumatoid disease.

The hypothesis is that iron, which accumulates in rheumatoid synovial membrane and fluid contributes to the variable expression of rheumatoid disease in two ways. Firstly, it catalyses oxidative radical reactions which lead to the formation of the hydroxyl radical and subsequent lipid peroxidation. Hydroxyl radicals and lipid peroxidation cause extensive disruption of cellular and organelle membranes and promote inflammatory tissue damage. Secondly, the infiltration of the rheumatoid synovium by chronic inflammatory cells may be due not to an antigenic process but to the tendency for these cells, which have receptors for iron-binding proteins, to migrate towards deposits of iron.

Acute Disease↗
PubMed1981

Superoxide-dependent formation of hydroxyl radicals in the presence of iron salts. Detection of 'free' iron in biological systems by using bleomycin-dependent degradation of DNA.

Bleomycin in the presence of iron(II) degrades DNA to form a thiobarbituric acid-reactive product. This has been made the basis of a specific assay method for 'free' iron in biological fluids. Human synovial fluid, human cerebrospinal fluid and rat pleural-exudate fluid were found to contain micromolar concentrations of 'free' iron, which would be sufficient to allow formation of the hydroxyl radical from superoxide and hydrogen peroxide generated in vivo. This assay method does not detect iron bound to transport proteins or to enzymes.

Bleomycin↗
PubMed1981

Iron--dioxygen-dependent changes to the biological activities of bleomycin.

Antitumor antibiotic bleomycin can bind to and degrade DNA, both in vivo and in vitro. This DNA damaging property in vitro can be related to its ability to chelate ferrous ions under aerobic conditions leading to the formation of "active oxygens," which are thought to be directly responsible for the damage. At present, evidence points to the hydroxyl radical formed by an iron-catalyzed Haber-Weiss reaction as the free radical most likely to be involved in this damage. When these same reactions occur in the absence of DNA, the free radicals then damage the bleomycin molecule, resulting in changes to its DNA-degrading activity, antibacterial properties, and chemical composition. Attempts to protect both bleomycin and DNA with a variety of specific and nonspecific scavengers have been unsuccessful, with several even showing pro-oxidant activity towards the iron-dependent damage. Only the metal chelators were effective inhibitors of bleomycin-iron-dependent damage to DNA. The damaged bleomycin lost some 50% of its ability to degrade DNA in vitro. This activity was closely paralleled by a loss in antibacterial activity against two different strains of bacteria.

Animals↗
PubMed1981

Protection against superoxide and hydrogen peroxide in synovial fluid from rheumatoid patients.

1. On exposure of synovial fluid to superoxide and hydrogen peroxide, generated enzymically or by activated polymorphonuclear leucocytes, hyaluronic acid is depolymerized and the fluid loses its lubricating properties. The ability of synovial fluid from rheumatoid patients to scavenge superoxide and hydrogen peroxide was therefore examined. 2. Synovial fluid from a range of rheumatoid patients contained no superoxide dismutase activity, insufficient caeruloplasmin to scavenge any superoxide radical and little, if any, catalase activity. 3. Total ascorbate (reduced ascorbate + dehydroascorbate) concentrations in the plasma and synovial fluid of rheumatoid patients were similar in each case. The values are at the low end of the normal range. 4. These results are discussed in relation to the role of oxygen radicals in inflammatory joint disease.

Arthritis, Rheumatoid↗